From an SBS piece: “Ms Radd said Teff is also nutritious and can be used for a variety of things.

‘It tends to be a bit higher in a trace element called Manganese, and Copper and it does have the nutrients that all the other whole grains have, which is protein, good carbohydrates and fibre and so on. But it also includes something called resistant starch.’

‘Now research on all whole grains has shown that fibre and resistant starch are incredibly important for our gut our bowel, because these components promote the growth of healthy bacteria which are known to be really important for our immunity. In fact they’re now saying that about 80 percent of our immunity in our body occurs at the gut level,’ she added.”

If you do go to an Ethiopian restaurant, which I highly recommend, make sure they have injera made with teff and not wheat. The place I go to has both, so make sure you ask.

My thesis is that if it is, it’s not because of anything Grace Liu of Animal Pharm is feverishly posting, in five parts so far. The time for vitriol and snark is over; so this time, it’s just the facts, ma’am, and you can judge for yourselves.

…I mean, really. If she’d just say, “I don’t recommend PS, I think there are better prebiotics,” then fine. I’d still think it plays a role, but whatever. Chocolate. Vanilla. But this endless cycle of “proof” that “PS is destroying gutz!!!” is quite ridiculous, smelling a lot more like a campaign to discredit those of us who’ve been advocating it than honest, science-based inquiry. Since I’m seeing little in the way of this “doctor’s” conclusions being challenged, I guess it’s time to do so semi-formally.

This addresses just the first part of the last of her posts on the topic: High Dose Potato Starch Can Make You Fatter, Insulin Resistant By Lowering GLP-1 AND ESPECIALLY If You Are Missing Bifidobacteria longum and Akkermansia mucinophila, aka SAD Microbial Fingerprint (Part V) NSFW (December 24, 2014).

Then she lists everything from Table 1 as “proof” that RS2 is bad vis-a-vis gut health or downstream consequences. The problem is, almost everything on that table is labelled NS, meaning not statistically significant. The few things that are not labelled NS, she misinterprets as BAD!!!

For instance: “OMG GLP-1 decreased!” But what does Bodinham actually say?

Fasting GLP1 concentrations were significantly lower (P=0.049) following HAM-RS2 compared with placebo; however, there was a significantly greater meal GLP1 excursion with HAM-RS2 than with the placebo (P=0.009; Fig. 1C). [emphasis added]

…and

Indeed, GLP1, a well-defined incretin, was found to be elevated postprandially after HAM-RS2 intake, again a finding which was not found in our previous published work in those without diabetes (23) but has been reported in studies of RS in animal models (24). Interestingly, there was no effect of this elevated GLP1 on postprandial insulin levels and so any effect on postprandial glucose disposal may have been through insulin-independent mechanisms. GLP1 has been shown to directly increase muscle glucose uptake in rodent models (25), with the GLP1 receptor recently localized to human skeletal muscle (26). GLP1 acutely raises nitric oxide (NO) levels and so acute changes in both microvascular recruitment (27) and endothelial function (28) at the level of the muscle are believed to be involved in this effect. In the current study, glucose uptake across forearm muscle measured directly using A-V sampling was increased following HAM-RS2 intake and against a background of elevated GLP1 (Fig. 1) [emphasis added]

So, while fasting levels were lower, the after-meal effect was higher. GLP-1 has a half-life of 1-5 minutes in the blood. The lowered fasting GLP-1 is probably a good thing, but seen simply as a curiosity by Bodinham. To make a lesser point, her series is about potato starch, not HAM (high amylose maize RS2).

And just as an aside—a lesson in dishonest manipulation—here’s the line item on pancreatic fat she makes a big—32.5% INCREASED, WTF!?!?!—deal of:

Beyond the fact that the non-significant findings overlap in potential +/-, if you wanted to manipulate someone, would you tell them they were driving 13 in a 10 zone, or that they were breaking the speed limit by over 32%!

In conclusion, this is the first RS feeding study in human T2DM where the metabolic effects of RS (rather than a manipulation of dietary glycemic index/glycemic load (37)) have been investigated. HAM-RS2 intake improved meal glucose tolerance in patients with existing good diabetic-control due to a mechanism which appears to involve increased muscle uptake of FAs and increased S-IMCL. However, as a caveat, changes in both ectopic TG distribution and plasma TG were found, the clinical significance of which is unknown. Further work is now warranted to elucidate the molecular mechanisms within muscle tissue attributable to HAM-RS2, which would be vital in terms of recommending diet/exercise interventions to maximize the benefits for muscle glucose uptake. A larger scale intervention should now be undertaken in patients using high-fiber foods, with less well-controlled diabetes and over a longer time frame before a change to the evidenced-based dietary guidelines could be proposed. [emphasis added]

Bodinham is saying he thinks that RS2 has further improved T2D in these subjects —just like we’ve been saying here for 2 years in over 100 posts—not destroyed them in any way…but there were a few metabolic changes they were not expecting to see. These were not normal, healthy, people…they all had diabetes and were either taking meds (15 out of 17 participants) or being controlled through diet and exercise (2/17):

All participants had well-controlled diabetes (mean HbA1c levels of 46.6 (s.e.m. 2) mmol/mol at screening) and were diet and exercise controlled (2/17), taking metformin (13/17) or metformin and pioglitazone (2/17), were weight stable, and excluded if they had a history of gastrointestinal, cardiovascular, or other endocrine diseases.

OK. Then she invokes an older study, same dude, Bodinham 2012. She does the same thing: takes Table 1 and makes all of the NS items sound like a death sentence. Unfortunately for her, the only thing on Table 1 that was really significant was a reduction in fasting glucose. She explains this is really—trust her—a bad thing. Yes, you’ll read that right:

Fasting glucose THIS TIME decreased BUT that is because all the spikes in post-prandial insulin is shoving all the glucose into adipose cells now and making them fatty which is clear by the increased TG and higher insulin-related consequences: higher systolic and diastolic blood pressures. wtf. I bet it lowered GLP1 where it is already low and lame in overweight and T2 diabetes subjects. [double emphasis added]

What did Bodinham say?

This study was designed to further explore the effects of HAM-RS2 on insulin secretion. To our knowledge this is the first study to demonstrate a significant improvement in first-phase insulin secretion following short-term supplementation with dietary fibre in the form of resistant starch (HAM-RS2). This work adds to our group’s previous findings of a positive effect of HAM-RS2 on insulin sensitivity. [emphasis added]

Let’s take another look at her GLP-1 “theory.” In this 2012 study just cited, Bodinham said:

However, whilst there are data from rodent studies showing increases in GLP-1 following RS intake [15]–[17] data confirming this effect in humans are lacking, and indeed, one study in humans has shown that it may take a year of increased fibre intake (increase of 20 g/day) to increase GLP-1 secretion.

But just 2 years later, in 2014, he did show that RS2 raised postprandial GLP-1 in the human T2D subjects. So, all of this GLP-1 “proof” is completely wrong, and seems intentionally misleading.

Indeed, GLP1, a well-defined incretin, was found to be elevated postprandially after HAM-RS2 intake, again a finding which was not found in our previous published work in those without diabetes… (Bodinham, 2014) [emphasis added]

Yet, here’s what she says says:

What is GLP1?

I love GLP-1.

It helps us to burn and remodel fat. “Glucagon-like peptide 1 (GLP-1), a gut-derived peptide, has been reported to have profound effects on metabolism and to reduce insulin resistance (Yang et al 2013).” High protein diets raise GLP-1 and satiating PYY gut hormones to cause nice fat burning. It appears that high dosage raw starches causes a downward trend of this fat-burning molecule. Ruh-OH. This time it does not depend on either the pre-existing gut or what human gut symbions are missing. It happens in healthy human subjects in several trials so far. [emphasis added]

So, she uses a guy’s study to try and “prove” what’s not proved, implying it’s relevant to healthy people; is going to make them fat, when it actually involved diabetic people and improved their status on balance. Then, she finally acknowledges the diabetic point, but only to make a false distinction in healthy people, claiming results that don’t actually exist.

OK, I think I’ve wasted enough time on this. Really, the whole post is a mess. The links don’t jive with what she’s saying. She’s just making stuff up, as in the foregoing. I suspect that a similar close examination of her Parts 1-4 are going to yield similar poison fruit. And, if you have a good memory, you might even remember when she wrote this in her own comments:

(Akkermansia is good for us ;) lol unless overgrown in defective barriers

So…

Unfortunately, so very many just read post titles, skim—maybe check a few sycophant comments—and chalk it up to another “excellent post” by the “Gut Goddess” Fake Doctor. In contrast, there are over 130 posts here on RS and GutGeneral, over 10,000 comments, over two years. The positive anecdotes of N=1,000+ are legion.

I can only conclude that she wants to stop or inhibit that for her own selfish gain, because she has statistically insignificant relevance to do with any shred of it. She’s made no long-term meaningful contributions—often inhibiting—but rather, only tried to dishonestly garner an unearned limelight.

Finally, she’s spent five posts on a straw man, because except for diabetics and those who insist on remaining VLC, high dose potato starch was never touted as the be-all-cure-all. Not even from the very first post on RS. I’ve addressed this before.

Now, this simply serves as something linkable next time someone asks me to address her idiotic posts that they don’t want to take the time to examine closely themselves.

I watch quite a bit of Food Network when I don’t really want to search for anything to watch, so it’s whatever comes up. One of the shows I tend to like best is Ina Garten’s Barefoot Contessa, at least when she prepares simple rustic cuisine.

So the other day, I saw her make a warm French lentil salad and had to give it a go myself. It’s super easy. Most curious about it is boiling the lentils with a whole peeled onion stabbed with cloves and a turnip cut in half (which are both discarded after cooking).

click to enlarge

Brining the lentils to a boil and immediately turning down to a light simmer, uncovered for 20 minutes, yielded perfect al dente lentils, ideal for a salad dish.

Yes, only 3 minutes for the carrots and leek, then another minute with the garlic (I used 4 cloves). Remove and let sit in the same pan until the lentils are done.

Soon as the lentils are done, drain and add them to the veggies, then stir in the dressing while it’s still hot.

If you taste it immediately it’s going to taste salty. Patience. After it settles, it’ll be perfect.

Click to enlarge

I found salmon to be a nice pairing, and you don’t even need to start it until the lentils are done and resting. Preheat your oven to 425. Pan fry the salmon on medium high, skin side down for 3 minutes. Then season with salt & pepper and drizzle some EVOO, and put the pan in the oven for 6 minutes.

Way back in 2007, Art De Vany used to talk about his glutathione supplements and upon looking into it, I heard from numerous sources that it’s simply not bioavailable taken orally. Glutathione is generally regarded as the body’s master anti-oxidant.

Glutathione (GSH) is an important antioxidant in plants, animals, fungi, and some bacteria and archaea, preventing damage to important cellular components caused by reactive oxygen species such as free radicals and peroxides.[2] It is a tripeptide with a gamma peptide linkage between the carboxyl group of the glutamate side-chain and the amine group of cysteine (which is attached by normal peptide linkage to a glycine).

It’s not an essential nutrient, since we synthesize it ourselves from the amino acids L-cysteine, L-glutamic acid, and glycine. So, two studies:

Longtime reader and email correspondent Scott Miller excerpted this from the full text of the first study.

…Witschi et al. (1992) have observed no increase in plasma GSH levels after a single oral supplementation of GSH to healthy human volunteers at 0.15 mmol/kg body weight. The present study confirmed these results [Figure 5(a) and (b)]. Based on these results, it has been suggested that the oral supplementation of GSH does not affect blood GSH levels.

It has been demonstrated that plasma proteins, including albumin, can bind to low molecular weight thiol-compounds through a disulfide bond. Therefore, there is the possibility that supplemented GSH may be transported as a conjugate of protein in the blood, and this has not been examined. In the present study, the effects of the supplementation of GSH on plasma protein-bound GSH levels were examined…

…The present study also demonstrated that only a negligible amount of GSH was bound to plasma protein before the supplementation of GSH. However, the protein-bound GSH significantly (P < 0.01) increased from 60 to 120 min after the oral supplementation of GSH. This is the first report to demonstrate an increase in GSH in the human blood fraction by the oral supplementation of GSH. The protein bound form GSH level in plasma after supplementation of GSH is much higher (>1000 times) than other food-derived peptides such as Val-Tyr 25 and Ile-Pro-Pro 26, but less than the food-derived collagen peptides in human blood.

It has been thought that orally administered GSH is successively degraded to cysteinyl-glycine, cysteine, and glycine by γ-glutamyl-transferase and peptidase. Cysteine could be used for GSH synthesis in cells. Increased levels of protein-bound GSH might be derived from the newly synthesized GSH. The present study also detected fragment peptide (Cys-Gly) and precursor peptide (γGlu-Cys) as protein-bound form in human blood, which suggests some GSH is synthesized from degradation products of GSH.

However, an early study by Kubo (1968) that used 35S-labeled GSH and paper electrophoresis has suggested that GSH could be directly absorbed from the small intestine into rat portal blood. Therefore, there is a possibility that supplemented GSH is directly absorbed into human blood and bound to plasma protein. To solve these problems, further studies on the metabolic fate of supplemented GSH that use 13C-labeled GSH are in progress…

And from the second study.

GSH levels in blood increased after 1, 3 and 6 months versus baseline at both doses. At 6 months, mean GSH levels increased 30-35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells in the high-dose group (P < 0.05). GSH levels increased 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P < 0.05). In most cases, the increases were dose and time dependent, and levels returned to baseline after a 1-month washout period. A reduction in oxidative stress in both GSH dose groups was indicated by decreases in the oxidized to reduced glutathione ratio in whole blood after 6 months. Natural killer cytotoxicity increased >twofold in the high-dose group versus placebo (P < 0.05) at 3 months.

Life Extension Glutathione, Cysteine and C, 750 mg. The question is, how much do you need, and is there a potential downside? It’s all very complicated, all intertwined—in my view—with hormesis, autophagy, apoptotic clearance, and the push-pull, yin-yang relationship between methylglyoxal and glutathione. I’m intuitively resistant to the idea that if some is good, more must be better. So many processes seem to have opposing counterparts—inflammation being a classic example. Yes, chronic inflammation is bad, but many forms of acute inflammation are beneficial. Negative feedback mechanisms are enhanced by opposing positive feedbacks, and vice-versa. It’s the way nature operates to balance on the head of a pin.

What Dr. Eades couldn’t have known, back in 2008, is that the same group of researchers (sans Jarrett) published another exciting paper in 2010—again with rats—showing that a ketogenic diet appears to produce its therapeutic benefits with a hormetic dose of oxidative stress, which activates the cytoprotective nuclear factor erythroid 2-related factor 2 (Nrf2)-signaling pathway. The Nrf2 pathway activates genes that are involved in detoxification of chemicals and antioxidant defense. That kind of stress is a good thing, at the right dose. The Nrf2 pathway itself is described by some as a key hormetic pathway and has been linked to longevity. And in fact, some studies suggest that trying to avoid low levels of oxidative stress is counterproductive.

…If you didn’t catch that, what this study showed is that chronic ketogenic diets (3 weeks) appear to deplete the liver of glutathione in the same way as taking Tylenol every day!

So, perhaps those most in need of supplementing glutathione, now that we know it’s bioavailable, would be those on low carb and ketogenic diets—as well as those who take Tylenol, or perhaps other analgesics or NSAIDs.

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I'm Richard Nikoley. Free the Animal began in 2003 and as of 2018, contains over 4,600 posts and 110,000 comments from readers. I cover a lot of ground, blogging what I wish...from health, diet, and lifestyle to philosophy, politics, social issues, and cryptocurrency. I celebrate the audacity and hubris to live by your own exclusive authority and take your own chances in life. [Read more...]

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